2023
MYC to BCL6 State-Transitions Determine Cell Size and Metabolic Fluctuations and Define a Novel Biorhythm in B-Cell Malignancies
Cheng Z, Kume K, Müschen M. MYC to BCL6 State-Transitions Determine Cell Size and Metabolic Fluctuations and Define a Novel Biorhythm in B-Cell Malignancies. Blood 2023, 142: 2769. DOI: 10.1182/blood-2023-190972.Peer-Reviewed Original ResearchGerminal center-derived B-cell lymphomaB cell developmentCell size fluctuationsCell cycleImmunoglobulin light chain gene recombinationDNA damage-induced apoptosisDistinct cellular statesNormal B cell developmentDamage-induced apoptosisExit cell cycleCell sizeB cell transitionGene expression profilesQuiescent phenotypeOncogenic tyrosine kinasesCell cycle arrestActivation of autophagySingle-cell sortingCellular statesCell divisionHigher glycolysis activityMYC transcriptionB cell cycleSuppression of glycolysisExpression profiles
2022
ACTR5 controls CDKN2A and tumor progression in an INO80-independent manner
Xu X, Chan A, Li M, Liu Q, Mattson N, Pokharel S, Chang W, Yuan Y, Wang J, Moore R, Pirrotte P, Wu J, Su R, Müschen M, Rosen S, Chen J, Yang L, Chen C. ACTR5 controls CDKN2A and tumor progression in an INO80-independent manner. Science Advances 2022, 8: eadc8911. PMID: 36563143, PMCID: PMC9788768, DOI: 10.1126/sciadv.adc8911.Peer-Reviewed Original ResearchCell cycle signalingCRISPR interference screenCell cycle machineryHallmark of tumorigenesisINO80 chromatinInterference screenEpigenetic regulatorsTumor progressionEpigenetic mechanismsCycle machineryEpigenetic dysregulationComplex membersTumor suppressorCell cycleCRISPR geneHCC tumor growthIes6CDKN2A expressionPharmacological inhibitionSignalingMultiple cancersHCC proliferationNovel opportunitiesTumor growthDynamic interplay
2012
Identification of FoxM1 As Therapeutic Target in TKI-Resistant Ph+ ALL
Buchner M, Klemm L, Zhengshan C, Geng H, Muschen M. Identification of FoxM1 As Therapeutic Target in TKI-Resistant Ph+ ALL. Blood 2012, 120: 874. DOI: 10.1182/blood.v120.21.874.874.Peer-Reviewed Original ResearchB cell precursorsLymphoblastic leukemiaTherapeutic targetPhiladelphia chromosome-positive acute lymphoblastic leukemiaPositive acute lymphoblastic leukemiaARF peptidesCell precursorsTreatment of TKIMajority of patientsTime of diagnosisAcute lymphoblastic leukemiaPatient-derived xenograftsValid therapeutic targetEffects of TKIsPotential therapeutic agentForkhead box transcription factor familyCell cycleSuperoxide dismutase expressionG0/G1Thiostrepton treatmentTKI treatmentPoor outcomeCombination therapyFl miceClinical trials
2011
Pre-B Cell Receptor-Mediated Activation of BCL6 Induces Pre-B Cell Quiescence Through Transcriptional Repression of MYC
Nahar R, Ramezani-Rad P, Mossner M, Duy C, Cerchietti L, Geng H, Jumaa H, Ye B, Melnick A, Muschen M. Pre-B Cell Receptor-Mediated Activation of BCL6 Induces Pre-B Cell Quiescence Through Transcriptional Repression of MYC. Blood 2011, 118: 1406. DOI: 10.1182/blood.v118.21.1406.1406.Peer-Reviewed Original ResearchPre-B cell receptorCell receptorCell cycle exitExit cell cycleInitial proliferative burstAcute lymphoblastic leukemiaCycle exitB cell precursorsPre-B cell receptor signalingInducible activationTranscriptional repressor BCL6Receptor-Mediated ActivationCell receptor signalingInduction of quiescenceLymphoblastic leukemiaCell surface expressionOverexpression of MYCCCND2 expressionCell cycleBcl6-deficient miceMalignant transformationReceptor signalingReceptors resultsCell precursorsReceptors